Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The in vivo mitogenic responses to lipopolysaccharide or concanavalin A by spleen cells of mice exposed to 20 ppm nitrogen dioxide (NO2) for 96 hr, were evaluated. [3H]Thymidine incorporation after addition of either mitogen, was significantly lower in spleen cells from acutely NO2-exposed mice (NO2 SC) than from control mice, although cell viability was not affected. T- and B-cell mitogenic responses were inhibited to the same extent by NO2 exposure. NO2 SC responses were protected by the thiol compounds 2-mercaptoethanol, L-cysteine, and selenomethionine. No restoration of mitogenic response was observed after treatment with reduced glutathione. Mechanisms accounting for this in vivo NO2 immune toxicity, are discussed in terms of oxidative injury.
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PMID:In vivo nitrogen dioxide exposure depresses spleen cell in vitro mitogenic responses: effects of sulfur compounds. 380 31

Human B lymphocytes, purified from the peripheral blood of several different donors can be pooled, frozen, and stored in liquid nitrogen to provide an easy and reproducible source of cells for mitogenic assays. These B cell preparations did not show any reactivity to T cell mitogens, but responded to Staphylococcus aureus Cowan strain 1 (SAC) and anti-IgM antibodies to the same extent as freshly purified B cells. When stimulated with either anti-IgM antibodies or SAC, these B cells became responsive to B cell growth factor (BCGF), allowing a quantitative measurement of this important lymphokine activity. In addition, we have studied the reactivity of frozen B lymphocytes to various combinations of activators. We have confirmed that phorbol myristate acetate (PMA) was a very potent mitogenic agent for preactivated human B cells and shown that bacterial lipopolysaccharide (LPS), although not mitogenic by itself, could synergize with anti-IgM antibodies to yield increased levels of stimulation. Furthermore experiments using the lysosomotropic agent leucine methyl ester showed that the action of LPS on anti-IgM-stimulated B cells did not require the presence of functional monocytes. Neither PMA nor LPS could induce BCGF responsiveness and thus these two compounds can be considered exclusive step 2 activators for human peripheral blood B cells.
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PMID:The reactivity of frozen B lymphocytes to B cell mitogens and human B cell growth factor: a study of step 1 and step 2 activators. 387 63

Estramustine, a nitrogen mustard derivative of estradiol-17 beta widely used for treatment of prostatic cancer, was found to inhibit the proliferative response of mouse lymphocytes to T (concanavalin A) and B (lipopolysaccharide) cell mitogens in vitro. Concanavalin A-induced lymphoproliferation was considerably more sensitive to the antiproliferative effect of estramustine than lipopolysaccharide-stimulated proliferation. The concentration of estramustine selectively inhibiting T lymphocyte proliferation was only active when present during the first 24 h of culture and could be overcome by exogenously added interleukin 2. Estramustine was shown to directly inhibit the production of interleukin 2 in concanavalin A-stimulated lymphocyte cultures without affecting the expression of interleukin 2 receptors. Thus the preferential inhibitory effect of estramustine on mitogen-induced T lymphocyte activation is apparently mediated by interference with the production or release of interleukin 2.
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PMID:Inhibition of T lymphocyte activation by estramustine: dose-dependent interference with IL-2 production and later proliferation events. 387 48

The lipopolysaccharide (LPS) from Rhizobium trifolii 0403 was isolated at different stages of growth and was examined for its (i) ability to bind a white clover lectin (trifoliin A), (ii) immunochemical properties, and (iii) composition. There was significantly more binding of trifoliin A to purified LPS and cells in the early stationary phase than to cells in the exponential phase. Immunofluorescence and enzyme-linked immunosorbent assays indicated that new antigenic determinants of the LPS appeared for brief periods on cells at the end of the lag phase and again at the beginning of the stationary phase. These new antigens were not detected on cells in midexponential or late stationary phase. Monovalent fragments of immunoglobulin G antibodies raised against the unique antigenic determinants in the LPS competitively blocked the binding of trifoliin A to cells in the early stationary phase. Gas chromatographic analysis showed that the relative quantity of several glycosyl components in the LPS increased as the culture advanced from the midexponential to the early stationary phase. In addition, LPS from cells in the early stationary phase had a higher aggregate molecular weight. Quinovosamine (2-amino-2,6-dideoxyglucose) was identified by combined gas chromatography-mass spectrometry as a sugar component of the LPS which had not been previously reported. D-Quinovosamine, N-acetyl-D-quinovosamine, and its n-propyl-beta-glycoside were effective hapten sugars which inhibited the binding of trifoliin A, anti-clover root antibody, and homologous antibody to these new determinants in the LPS. White clover plants had more infected root hairs after incubation with an inoculum of cells in the early stationary phase than after incubation with cells in the midexponential phase. The profound influence of the growth phase on the composition of lectin-binding polysaccharides of Rhizobium may be a major underlying cause of conflicting data among laboratories testing the lectin-recognition hypothesis. In addition, these chemical modifications may reflect mechanisms which regulate Rhizobium-root hair recognition in this nitrogen-fixing symbiosis.
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PMID:Growth-phase-dependent immunodeterminants of Rhizobium trifolii lipopolysaccharide which bind trifoliin A, a white clover lectin. 617 Jun 30

T-2 toxin, a trichothecene mycotoxin, is a potently cytotoxic and immunosuppressive secondary metabolite produced by Fusarium fungi. Young male white Swiss mice were fed a diet supplemented with T-2 toxin at levels of 5, 10, or 20 ppm, control diet ad libitum, or control diet at a restricted rate for 1, 2, 3, 4, and 6 weeks. The effect of the toxin on the immune system of these mice was assessed by counting total spleen cell numbers and the in vitro proliferative response of spleen cells from these mice to the polyclonal mitogens, concanavalin A (Con A), and lipopolysaccharide (LPS). Body weight gains were also measured. Initially, the ingestion of T-2 toxin and restricted diet depressed total spleen cell counts, but after 3 weeks, only the spleen cell counts of mice fed 20 ppm of T-2 toxin were significantly lower. Consumption of 20 ppm of T-2 toxin by mice for 1 to 4 weeks depressed the spleen proliferative responses to the T-cell mitogen Con A; however, the response to LPS, a B-cell mitogen, was depressed in mice fed 10 and 20 ppm of T-2 toxin as well as in mice fed a control diet at a restricted rate. In order to determine whether T-2 toxin could induce reactivation of herpes simplex virus type 1 (HSV-1), latency was established in the trigeminal ganglia of mice. Feeding of T-2 toxin at 5, 10, and 20 ppm levels for 3 or 6 weeks did not reactivate virus; however, treatment with liquid nitrogen and cyclophosphamide did reactivate virus. These results demonstrate that although T-2 can cause immunosuppression, this response is not sufficient to reactivate HSV-1.
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PMID:The effects of dietary T-2 toxin on the immunological function and herpes simplex reactivation in Swiss mice. 630 70

Escherichia coli F-18, isolated from the feces of a healthy human, is an excellent colonizer of the large intestines of streptomycin-treated CD-1 mice. E. coli F-18 Col-, a poor mouse colonizer relative to F-18, lacks a 3 X 10(7)-dalton plasmid present in E. coli F-18. Both strains are human type A erythrocyte hemagglutination negative, have identical surface hydrophobicities, contain the same number of lipopolysaccharide molecules with the same O-side chain length, and have identical amounts of capsule. Differences between the two strains were observed. The relative amounts of specific outer membrane proteins differed, and E. coli F-18 was less motile than E. coli F-18 Col-. The abilities of the two strains to bind mouse large intestine mucous gel was also examined. Although each strain was able to use mucous gel as the sole source of carbon and nitrogen with equal ability, E. coli F-18 bound between two and three times more mucous gel than did E. coli F-18 Col-. Most of the difference in mucous gel binding ability of the two strains was accounted for by the greater ability of E. coli F-18 lipopolysaccharide to bind a single 26,000-dalton mucous gel protein. E. coli J5-3, a typical K-12 strain that is also a poor colonizer relative to E. coli F-18, was identical to E. coli F-18 Col- with respect to mucous gel binding ability.
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PMID:Relationship between the mouse colonizing ability of a human fecal Escherichia coli strain and its ability to bind a specific mouse colonic mucous gel protein. 633 11

Incorporation of an oral dose of [15N]ammonium acetate into urinary [15N]nitrate has been demonstrated in the rat. Investigation of the regulation of nitrate synthesis has shown that Escherichia coli lipopolysaccharide potently stimulates urinary nitrate excretion (9-fold increase). It was further shown that the enhanced rate of nitrate excretion by lipopolysaccharide was due not to a reduction in nitrate metabolic loss but rather to an increased rate of synthesis. This conclusion was based on finding a proportionally increased incorporation of [15N]ammonium into nitrate nitrogen with lipopolysaccharide treatment. Nitrate biosynthesis was also increased by intraperitoneal injection of carrageenan and subcutaneous injection of turpentine. It is proposed that the pathway of nitrate biosynthesis may be the result of oxidation of reduced nitrogen compounds by oxygen radicals generated by an activated reticuloendothelial system.
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PMID:Mammalian nitrate biosynthesis: incorporation of 15NH3 into nitrate is enhanced by endotoxin treatment. 634 71

The metabolic fate of an oral dose of 3.5 mmol 15N-labelled nitrate was investigated in young adults. An average of 60% of the 15N-nitrate dose appeared in the urine within 48 h; less than 0.1% appeared in the faeces. Some of the 15N label of nitrate was found in the urine (3%) and faeces (0.2%) in the form of ammonia and urea; the remainder of the dose was attributed to nitrate loss via metabolism to other reduced nitrogen compounds. Studies with germ-free rats indicated that half of the nitrate metabolism is due to mammalian processes. These and previous studies show that not all of the nitrate excreted in the urine is of dietary origin but evolves from endogenous synthesis. An oral dose of 15N-ammonium acetate was incorporated into urinary 15N-nitrate in rats, suggesting that ammonia is a precursor of nitrate. Furthermore, Escherichia coli lipopolysaccharide was found to be a potent stimulus of nitrate excretion (nine-fold increase), due to an increased rate of synthesis. Two other types of experimentally induced inflammatory states - injection of carrageenan and of turpentine - enhanced nitrate synthesis. It is proposed that the pathway of nitrate biosynthesis may be the result of oxidation of reduced nitrogen compounds by oxygen radicals generated by an activated reticuloendothelial system.
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PMID:Mammalian nitrate biochemistry: metabolism and endogenous synthesis. 653 15

Palmerston North (PN) mice, a newly recognized model of systemic lupus erythematosus, were compared with autoimmune hybrid NZB/NZW mice in a study designed to examine spleen cell responsiveness to T-cell and B-cell mitogens. Modest reductions of responses to phytohemagglutinin (PHA) and concanavalin A (Con A) were noted in PN females after 24 weeks of age; these responses were reduced significantly in NZB/NZW females. In contrast, male PN and NZB/NZW mice responded actively to PHA and Con A throughout the first year of life. Responses to lipopolysaccharide were not affected by age or sex. Anti-DNA antibody levels, blood urea nitrogen, and glomerular histology were analyzed to determine if autoantibody production or renal failure correlated with suppressed mitogenic responsiveness. These factors, examined singly and together, were not as important as age. In this system, age and sex did not influence spleen cell responses to mitogens in normal CD-1 mice. Age and sex were of minimal importance in determining responses to T-cell mitogens in the recently defined PN model of autoimmunity. In contrast, age and sex exerted strong influences upon responses to PHA and Con A in the NZB/NZW model of lupus.
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PMID:Responses to T-cell and B-cell mitogens in autoimmune Palmerston North and NZB/NZW mice. 660 3

Rat alveolar macrophages (AM) were exposed in vivo or in vitro to nitrogen dioxide (NO2) and subsequently tested for phagocytic and tumoricidal activities. AM obtained by lavage from Fischer 344/N rats exposed for 4 h to 40 ppm NO2 were significantly more phagocytic to opsonized sheep red blood cells (SRBC), exhibited an increased cytotoxic response toward syngeneic mammary adenocarcinoma cells, and were more sensitive to activation by agents such as lipopolysaccharide, muramyl dipeptide, and macrophage-activating factor, as compared with the response of AM obtained from unexposed control rats. Repeated 4 h/d NO2 exposures over 7-d or 14-d periods usually resulted in AM activity similar to control levels, with some instances of increased phagocytic activity of the AM but not to the extent of that observed for a single 4 h exposure. There were no significant decreases in the cytotoxic or phagocytic activities of the AM during any of the exposure periods. For the in vitro exposures, AM were lavaged from normal rats and then exposed for various periods to 10, 20, or 40 ppm NO2. A dose-related and time-dependent enhanced cytotoxic response of AM was observed. Maximum AM-mediated cytotoxicity occurred after an in vitro exposure to 10 ppm NO2 for 2 h. The cytotoxic response was directed toward syngeneic mammary adenocarcinoma cells but not against syngeneic embryoblast cells, indicating that the AM retained the ability to distinguish between normal and abnormal cells. No inhibitory effects of NO2 on AM-mediated cytotoxicity were observed. These experiments suggest that the host AM-mediated immune defense of the lung may be modulated by host exposure to inhaled chemicals.
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PMID:In vivo and in vitro NO2 exposures enhance phagocytic and tumoricidal activities of rat alveolar macrophages. 682 22


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